Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
Human CDK5 Protein expressed in Wheat germ - ABIN1348956
Seo, Kim, Bae, Soh, Lee: Cdk5-mediated phosphorylation of c-Myc on Ser-62 is essential in transcriptional activation of cyclin B1 by cyclin G1. in The Journal of biological chemistry 2008
SNHG20 could function as an oncogenic long non-coding RNA by regulating miR (show MLXIP Proteins)-140-5p-ADAM10 (show ADAM10 Proteins) axis and MEK (show MAP2K1 Proteins)/ERK (show EPHB2 Proteins) signaling pathway in cervical cancer.
restoration of ADAM10 (show ADAM10 Proteins) expression partially reversed the effects of miR152 on cell proliferation and apoptosis in rheumatoid arthritisfibroblastlike synoviocytes.
Mechanisms underlying ADAM10 (show ADAM10 Proteins) downregulation by miR (show MLXIP Proteins)-140-5p and suggests that dysfunctional regulation of ADAM10 (show ADAM10 Proteins) expression is exacerbated by AD-related neurotoxic effects.
elevated expression of ADAM10 (show ADAM10 Proteins) was associated with the pathogenesis and development of immune thrombocytopenia
Report overexpression of ADAM10 (show ADAM10 Proteins) in oral squamous cell carcinomas, especially in OSCC with metastasis.
High ADAM10 (show ADAM10 Proteins) expression is associated with meningococcal purpura fulminans.
The findings of the present study suggested that miR320a may function as a tumor suppressor in GC progression and potential therapeutic strategies for GC may be based on the miR320a/ADAM10 (show ADAM10 Proteins) axis.
Insulin-like growth factor-1 (show IGF1 Proteins) activates different catalytic subunits p110 (show CUX1 Proteins) of PI3K (show PIK3CA Proteins) in a cell-type-dependent manner to induce lipogenesis-dependent epithelial-mesenchymal transition through the regulation of ADAM10 (show ADAM10 Proteins) and ADAM17 (show ADAM17 Proteins).
Methamphetamine can impair the endoplasmic reticulum-associated degradation pathway and induce neuronal apoptosis through endoplasmic reticulum stress, which is mainly mediated by abnormal CDK5-regulated Tau phosphorylation.
Mcl-1 (show MCL1 Proteins) is a disease-specific target of Cdk5, which associates with Cdk5 under basal conditions, but is not regulated by it.
these results indicate that phosphorylation of CHIP at Ser20 by Cdk5 activation inhibits CHIP-mediated truncated apoptosis-inducing factor (show AIFM1 Proteins) (tAIF) degradation, thereby contributing to tAIF-induced neuronal cell death following rotenone treatment
Identification of candidate lncRNAs regulated by Cdk5 in mouse skin.
These results of this study suggest that a physiological role of Cdk5 in visual cortex is to consolidate and stabilize neural circuits through controlling GABAergic signaling.
Selective loss of Cdk5 in dorsolateral striatum increased locomotor activity and attenuated motor learning.
CDK5-mediated phosphorylation of Sirt2 (show SIRT2 Proteins) has a role in to depressive-like behavior induced by social defeat stress
findings collectively demonstrate that the Cdk5-dependent phosphorylation of liprinalpha1 is important for the postsynaptic organization during activity-dependent synapse development.
Study generated Purkinje cell-specific p35 (show CDK5R1 Proteins); p39 (show ATP6V0D1 Proteins) double knockout, L7cre-p35f/f; p39 (show ATP6V0D1 Proteins)-/- mice and found there were ectopic Purkinje cells scattered singly or in groups over the cerebellar cortex due to Cdk5-loss-dependent migration failure. Selective loss of Cdk5 activity in Purkinje cells contributed to motor impairments. TrkB (show NTRK2 Proteins) agonist treatment partially rescued Purkinje cell morphological defects of dendritic structures.
Stress-induced nuclear translocation of CDK5 suppresses neuronal death by downregulating ERK activation via VRK3 phosphorylation
hyperactivation of p25 may temporarily enhance neural progenitor cell proliferation, but impair their long-term survival
These data indicate that Cdk5 is required to maintain the protective role of basal autophagy in the initial responses to a subset of neurodegenerative challenges via phosphorylating Acinus (show ACIN1 Proteins) at serine 437.
These data show that Cdk5 regulates the onset and extent of remodeling of the Drosophila mushroom body.
The CDK5 phosphorylates MEKK1 (show MAP3K1 Proteins), and together, they activate the JNK (show MAPK8 Proteins) pathway for apoptosis.
The data of this study demonstrated that Cdk5/p35 (show RPLP0 Proteins) kinase is a key regulator of the development and maintenance of the axon initial segment in Drosophila.
Therefore, we propose that Abl and p35/p25 (show CDK5R1 Proteins) cooperate in promoting Cdk5-pY15, which deregulates Cdk5 activity and subcellular localization in Abeta42-triggered neurodegeneration.
Cdk5/p35 (show RPLP0 Proteins) did not have major effects on tau toxicity or phosphorylation.
In Drosophila the cdk5 is needed for locomotive behavior and NMJ elaboration.
data indicate that PP1alpha is a downstream target of the NGF/Egr-1/Cdk5 pathway during NGF-induced differentiation of PC12 cells and suggest that PP1 phosphorylation promotes neuronal differentiation
The intrahepatic biliary network is a highly branched three-dimensional network lined by biliary epithelial cells. We designed a new computer-based algorithm that quantitatively computes the structural differences of the three-dimensional networks. Utilizing the algorithm, we showed that inhibition of Cyclin-dependent kinase 5 (Cdk5) led to reduced branching in the intrahepatic biliary network.
These results suggest that the phosphorylation of Dpysl2 (show DPYSL2 Proteins) and Dpysl3 (show DPYSL3 Proteins) by Cdk5 and DYRK2 (show DYRK2 Proteins) is required for the proper positioning of Rohon-Beard neurons and neural crest cells during neurulation in zebrafish embryos.
cdk5 mRNA was injected into the one- to two-cell embryos, in which neuron apoptosis was inhibited compared with the uninjected control embryos.
we have cloned and characterized the zebrafish cdk5 ortholog. Zebrafish cdk5 is 96% identical to its human counterpart and expressed as early as the blastula stage.
cdk5 plays a critical role in spinal and cranial motor neuron development.
CDK5-mediated hyperphosphorylation of SIRT1 (show SIRT1 Proteins) facilitates the development of endothelial senescence and atherosclerosis.
CDK5 mRNA reaches the highest level in cerebral cortex at two months of age and in cerebellum and liver at 4 months of age, respectively, whereas the peak level of CDK5R1 (show CDK5R1 Proteins) was observed in both cerebral cortex and cerebellum at two months of age
CDK-5 regulates DCV polarity by both promoting DCV trafficking in axons and preventing dynein-dependent DCV trafficking into dendrites.
Cdk-5 facilitates new synapse formation by regulating the transport of synaptic vesicles to the sites of synaptogenesis.
CDK-5 promotes the anterograde trafficking of GLR-1 and that phosphorylation of LIN-10 may play a role in this process.
Proline-directed serine/threonine-protein kinase essential for neuronal cell cycle arrest and differentiation and may be involved in apoptotic cell death in neuronal diseases by triggering abortive cell cycle re-entry. Interacts with D1 and D3- type G1 cyclins. Phosphorylates SRC, NOS3, VIM/vimentin, p35/CDK5R1, MEF2A, SIPA1L1, SH3GLB1, PXN, PAK1, MCAM/MUC18, SEPT5, SYN1, DNM1, AMPH, SYNJ1, CDK16, RAC1, RHOA, CDC42, TONEBP/NFAT5, MAPT/TAU, MAP1B, histone H1, p53/TP53, HDAC1, APEX1, PTK2/FAK1, huntingtin/HTT, ATM, MAP2, NEFH and NEFM. Regulates several neuronal development and physiological processes including neuronal survival, migration and differentiation, axonal and neurite growth, synaptogenesis, oligodendrocytes differentiation, synaptic plasticity and neurotransmission, by phosphorylating key proteins. Activated by interaction with CDK5R1 (p35) and ATP6V0D1 (p39), especially in post-mitotic neurons, and promotes CDK5R1 (p35) expression in an autostimulation loop. Phosphorylates many downstream substrates such as Rho and Ras family small GTPases (e.g. PAK1, RAC1, RHOA, CDC42) or microtubule-binding proteins (e.g. MAPT/TAU, MAP2, MAP1B), and modulates actin dynamics to regulate neurite growth and/or spine morphogenesis. Phosphorylates also exocytosis associated proteins such as MCAM/MUC18, SEPT5, SYN1, and PCTAIRE 1/CDK16 as well as endocytosis associated proteins such as DNM1, AMPH and SYNJ1 at synaptic terminals. In the mature central nervous system (CNS), regulates neurotransmitter movements by phosphorylating substrates associated with neurotransmitter release and synapse plasticity\; synaptic vesicle exocytosis, vesicles fusion with the presynaptic membrane, and endocytosis. Promotes cell survival by activating anti-apoptotic proteins BCL2 and STAT3, and negatively regulating of JNK3/MAPK10 activity. Phosphorylation of p53/TP53 in response to genotoxic and oxidative stresses enhances its stabilization by preventing ubiquitin ligase-mediated proteasomal degradation, and induces transactivation of p53/TP53 target genes, thus regulating apoptosis. Phosphorylation of p35/CDK5R1 enhances its stabilization by preventing calpain-mediated proteolysis producing p25/CDK5R1 and avoiding ubiquitin ligase-mediated proteasomal degradation. During aberrant cell-cycle activity and DNA damage, p25/CDK5 activity elicites cell-cycle activity and double-strand DNA breaks that precedes neuronal death by deregulating HDAC1. DNA damage triggered phosphorylation of huntingtin/HTT in nuclei of neurons protects neurons against polyglutamine expansion as well as DNA damage mediated toxicity. Phosphorylation of PXN reduces its interaction with PTK2/FAK1 in matrix-cell focal adhesions (MCFA) during oligodendrocytes (OLs) differentiation. Negative regulator of Wnt/beta-catenin signaling pathway. Activator of the GAIT (IFN-gamma-activated inhibitor of translation) pathway, which suppresses expression of a post-transcriptional regulon of proinflammatory genes in myeloid cells\; phosphorylates the linker domain of glutamyl-prolyl tRNA synthetase (EPRS) in a IFN-gamma- dependent manner, the initial event in assembly of the GAIT complex. Phosphorylation of SH3GLB1 is required for autophagy induction in starved neurons. Phosphorylation of TONEBP/NFAT5 in response to osmotic stress mediates its rapid nuclear localization. MEF2 is inactivated by phosphorylation in nucleus in response to neurotoxin, thus leading to neuronal apoptosis. APEX1 AP-endodeoxyribonuclease is repressed by phosphorylation, resulting in accumulation of DNA damage and contributing to neuronal death. NOS3 phosphorylation down regulates NOS3-derived nitrite (NO) levels. SRC phosphorylation mediates its ubiquitin- dependent degradation and thus leads to cytoskeletal reorganization. May regulate endothelial cell migration and angiogenesis via the modulation of lamellipodia formation. Involved in dendritic spine morphogenesis by mediating the EFNA1- EPHA4 signaling.
TPKII catalytic subunit
, cell division protein kinase 5
, protein kinase CDK5 splicing
, serine/threonine-protein kinase PSSALRE
, tau protein kinase II catalytic subunit
, CR6 protein kinase
, proline-directed protein kinase 33 kDa subunit
, neuronal cyclin-dependent kinase 5
, Cell division protein kinase 5
, cyclin-dependent-like kinase 5